In this paper we have attempted to describe the manner of spread of an endemic, native, respiratory infection and a method for its control. The essential factor determining the prevalence of such an endemic disease is, we believe, host susceptibility, which is controlled by hereditary and environmental influences. Furthermore, it seems probable that the amount of this population susceptibility determines the dosage of specific microbes available to the population.

An increase in dosage in the herd is followed by an increase in the spread and severity of the infection, and a decrease by a corresponding alleviation. Hence, two methods for the prevention of epidemics are available: (1) an enhancement of population resistance, and (2) the reduction to a minimum of available dosage. These procedures have proved successful for 3 years in maintaining a population of breeding rabbits, in the midst of a badly infected community, entirely free from Bact. lepisepticum infection.

Confirmation of the above conclusions has been gained from other studies in the field of experimental epidemiology. Dr. D. T. Smith (2), at Saranac, New York, found that changes in population susceptibility were responsible for a severe outbreak of Bact. lepisepticum infection and septicemia. Freund (3), at Berlin, has just published an interesting account of respiratory epidemics of rabbits and guinea pigs, apparently brought about by sudden changes in temperature and housing conditions. Pneumonia and Pasteurella infection, endemic in the population, increased suddenly in extent and severity. Nevertheless, neither endemic nor epidemic strains of the microorganisms were found to be especially virulent. Dr. Theobald Smith (4), in a study of paratyphoid epidemics of guinea pigs, has made similar observations. He noted that pregnant females acted as the foci of infection, and that from these individuals, presumably of lessened resistance, the bacteria were given off and infection was spread.

The studies in experimental epidemiology are rapidly reaching a stage where they may be applied to the problems of human disease. Indeed, more recent observations of the mode of spread of pneumonia (5–7), scarlet fever (8), typhoid (9, 10), plague (11), diphtheria (12–14), measles (15), and tuberculosis (16–18) increasingly show a tendency to discard the theory of fluctuating microbic virulence and to emphasize the importance of the host factors.

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